In a healthy heart, a heartbeat originates in the RA in the sinoatrial (“SA”) node. Activation spreads quickly across the atria to the atrioventricular (“AV”) node, which then delays the wave of excitation. The delay enables the atria to contract before the ventricles contract. After the activation is delayed by, and leaves, the AV node, it enters and excites the bundle of His. This excitation of the bundle of His spreads in a precise pattern to the ventricles through the ventricular conduction system composed of Purkinje fibers. Excitation spreading through this system activates each ventricular cell at a precise time to produce a coordinated ventricular contraction.
For various reasons, the AV node can be blocked (referred to as “AV block”), thus inhibiting or preventing utilization of the normal conduction system of the heart. AV block can also be therapeutically induced for rate control in patients with atrial fibrillation.
Ventricular pacing has been used for treating heart rhythm disorders when the normal conduction system of the heart can not be utilized due to AV block. However, ventricular pacing does not provide a high degree of electrical synchrony in the ventricular cells that is required for optimal mechanical function of the heart. As has been recently discovered, over long term, this can result in an increased occurrence of congestive heart failure.
One specific type of ventricular pacing is pacing from the right ventricular (“RV”) apex of the heart. RV pacing has been used due to the stability of the type of lead and the ease of lead placement. Examples of venous pacing leads and electrodes for RV pacing are described in U.S. Pat. No. 6,094,596. However, direct RV pacing can lead to suboptimal ventricular performance, such as desynchronized contractions, negative inotropic effects, histological and ultrastructural changes in ventricular tissue, risks of congestive heart failure complications, and even death.
Due to these drawbacks of RV pacing, alternative pacing sites, such as the RV outflow tract (“RVOT”) and various septal sites, have been explored to improve cardiac hemodynamics during pacing. Further, resynchronization therapy has been advanced by utilizing multiple ventricular pacing sites, such as biventricular pacing. However, the required physiological degree of synchrony may not be achieved using these alternative pacing methods. In addition, the clinical consequences of RVOT pacing are unknown.
Direct His bundle pacing has also been used in an attempt to achieve synchronized ventricular contraction in patients with an intact ventricular conduction system. However there can be limitations associated with His bundle pacing in humans. For example, studies have reported difficulty in pacing the relatively small area of the His bundle and difficulty inserting a pacing lead into the membranous septum. Further, higher pacing and lower sensing thresholds can be required for His pacing than for RV pacing due to the high fibrous content of the His region. Also, because His bundle pacing site is located close to aorta, there are potential, devastating consequences of damage of the aorta.
Accordingly there is a need for improved cardiac pacing devices and methods overcoming the deficiencies with conventional cardiac pacing.